Changes to AIDS dementia complex in the era of highly... : AIDS (original) (raw)

Epidemiology and Social: Original Papers

Changes to AIDS dementia complex in the era of highly active antiretroviral therapy

Dore, Gregory J.a; Correll, Patricia K.a; Li, Yueminga; Kaldor, John M.a; Cooper, David A.ab; Brew, Bruce J.abc

From the aNational Centre in HIV Epidemiology and Clinical Research, University of New South Wales, Darlinghurst, NSW, Australia; bHIV Medicine Unit, and cDepartment of Neurology, St Vincent‚s Hospital, Darlinghurst, NSW, Australia.

Sponsorship: The National Centre in HIV Epidemiology and Clinical Research is supported by the Commonwealth Department of Health and Family Services, through the Australian National Council on AIDS and Related Diseases and its Research Advisory Committee.

Correspondence to: Dr Gregory J. Dore, National Centre in HIV Epidemiology and Clinical Research, University of New South Wales, Level 2, 376 Victoria Street, Darlinghurst, NSW, 2010, Australia. Tel: +61-2-9332-4648; fax: +61-2-9332-1837; email: [email protected]

Received: 3 February 1999; revised: 29 March 1999; accepted: 7 April 1999.

Abstract

Objectives:

To determine the protective efficacy of highly active antiretroviral therapy (HAART) against AIDS dementia complex (ADC) relative to other initial AIDS-defining illnesses (ADIs), Australian AIDS notification data over recent years were examined.

Methods:

All initial ADIs in Australia over the period 1992-1997 were included. Three initial ADI groups were established: ADC; other predominantly central nervous system (CNS) ADIs (toxoplasmosis and cryptococcosis); and non-CNS ADIs. For each ADI grouping, the proportion of total ADIs, and median CD4 cell count in the pre-HAART era (1992-1995) were compared with the HAART era (1996 and 1997).

Results:

Initial ADIs peaked in Australia in 1994 (n=1049), with a gradual decline to 1996 (n=722), and a marked decline in 1997 (n=367). ADC constituted 4.4% of initial ADIs over the period 1992-1995, but increased after the introduction of HAART to 6.0% in 1996 and 6.5% in 1997 (_P_=0.02). In contrast, the proportion of other CNS ADIs (1992-1995, 8.1%; 1996, 6.0%; 1997, 8.2%; _P_=0.41) was stable over the period 1992-1997. The median CD4 cell count at ADC diagnosis increased from 70/mm3 in 1992-1995 to 120/mm3 in 1996 and 170/mm3 in 1997 (_P_=0.04). Although the median CD4 cell count also increased significantly over this period for both other CNS ADIs (40-60/mm3; _P_=0.02), and non-CNS ADIs (60-70/mm3; _P_=0.02), the increase was small.

Conclusion:

A proportional increase in ADC compared with other ADIs and a marked increase in the median CD4 cell count at ADC diagnosis have occurred since the introduction of HAART in Australia. These changes suggest that HAART has a lesser impact on ADC than on other ADIs, with the poor CNS penetration of many antiretroviral agents a possible explanation.